Thiamine (vitamin B1) is essential for oxidative metabolism and neuronal energy homeostasis. Its deficiency affects both the central and peripheral nervous systems, producing Wernicke’s encephalopathy (WE) and dry beriberi, respectively. These manifestations differ in tempo and tissue vulnerability: peripheral neuropathy evolves insidiously over weeks to months, whereas WE emerges acutely when deficiency becomes critical or metabolic demands increase. The coexistence of WE and dry beriberi is uncommon and may mimic inflammatory, infectious, or paraneoplastic disorders, delaying recognition of this reversible nutritional syndrome. 

A 37-year-old woman presented with three months of progressive bilateral leg weakness, sensory loss, bowel and bladder dysfunction, recurrent vomiting, and >25-lb weight loss. Examination revealed flaccid paraparesis with areflexia, a T12 sensory level, impaired short-term memory, and horizontal and vertical nystagmus with left lateral rectus palsy. MRI brain and spine were unremarkable. Electrodiagnostic studies showed symmetric, subacute, distal sensorimotor axonal polyneuropathy without demyelination. Serum thiamine was <6 µg/L. After intravenous thiamine, cognition and ocular motility improved within days, while motor recovery was slower and incomplete. Classic precipitants such as alcohol use or bariatric surgery were absent. The most plausible etiology was prolonged vomiting with reduced intake; low positive β-hCG suggested a resolving early pregnancy without clear cause.